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To describe changes in household access to iodized salt in relation to socioeconomic factors.We extracted data on iodized household salt from Multiple Indicator Cluster Surveys conducted in 2000 and 2010. As part of the surveys, household salt samples were tested for iodization by standardized rapid-test kits that yield results to indicate whether salt is not iodized, inadequately iodized, (less than 15 parts per million, ppm), or adequately iodized (more than 15 ppm). We calculated indices of household salt iodization in 2000 and 2010, taking into account survey sampling weights. We explored associations between these indices and socioeconomic variables, both within and between countries.We analysed data from 105 162 households in 2000 and 144 018 households in 2010. Between 2000 and 2010, household coverage of adequately iodized salt increased by 6.1% (from 46.3% to 52.4%) on average, but with regional differences: coverage fell by 13.0% (from 77.5% to 64.5%) in the Central African Republic but improved by 40.4% (from 22.2% to 62.6%) in Sierra Leone. Improvements in coverage were higher in rural areas and among the poorest households, but within-country socioeconomic disparities remained. There were weak associations between changes in salt iodization and national level socioeconomic indicators.Overall, the coverage of adequately iodized household salt increased over the last decade. However, the changes varied widely among countries. The goal of universal salt iodization is still distant for many countries and requires renewed efforts by governments, bilateral and multilateral agencies and civil society.Décrire les changements survenus dans l'accès des ménages à du sel iodé par rapport à divers facteurs socioéconomiques.Nous avons extrait des données sur le sel de cuisine iodé d'enquêtes par grappes à indicateurs multiples menées en 2000 et 2010. Dans le cadre de ces enquêtes, l'iodation d'échantillons de sel de cuisine a été évaluée à l'aide de kits de tests rapides standardisés qui ont permis d'obtenir des résultats indiquant que le sel n'est pas iodé, insuffisamment iodé (moins de 15 parties par million, ppm) ou suffisamment iodé (plus de 15 ppm). Nous avons calculé les indices d'iodation du sel de cuisine en 2000 et 2010 en tenant compte des poids d'échantillonnage des enquêtes. Nous avons examiné les liens entre ces indices et plusieurs variables socioéconomiques dans et entre les pays.Nous avons analysé des données provenant de 105 162 ménages en 2000 et 144 018 ménages en 2010. Entre 2000 et 2010, le nombre de ménages consommant du sel suffisamment iodé a augmenté de 6,1% (de 46,3% à 52,4%) en moyenne, mais des différences régionales ont été constatées: ce taux a baissé de 13,0% (de 77,5% à 64,5%) en République centrafricaine, mais a augmenté de 40,4% (de 22,2% à 62,6%) en Sierra Leone. Il a été noté que les améliorations étaient plus importantes dans les zones rurales et au sein des ménages les plus pauvres, mais que des disparités socioéconomiques subsistaient au sein des pays. Les liens entre les changements dans l'iodation du sel et les indicateurs socioéconomiques au niveau national se sont révélés faibles.Dans l'ensemble, l'accès à du sel de cuisine suffisamment iodé s'est amélioré au cours de la dernière décennie. Il a cependant été observé que les changements variaient considérablement d'un pays à l'autre. Dans de nombreux pays, l'objectif de l'iodation universelle du sel est loin d'être atteint et exige des gouvernements, des organismes bilatéraux et multilatéraux et de la société civile qu'ils renouvellent leurs efforts.Describir los cambios del acceso doméstico a sal yodada en relación con factores socioeconómicos.Se extrajeron datos sobre la sal doméstica yodada de encuestas de indicadores múltiples a nivel de grupos realizadas en 2000 y 2010. Como parte de las encuestas, se analizaron las muestras de sal doméstica para comprobar su yodación mediante kits de pruebas rápidas estandarizadas, cuyos resultados indicaron si la sal no estaba yodada, estaba insuficientemente yodada, menos de 15 partes por millón (ppm) o suficientemente yodada (más de 15 ppm). Se calcularon los índices de yodación de la sal doméstica en el 2000 y el 2010, teniendo en cuenta las ponderaciones de muestreo de las encuestas. Se exploraron las relaciones entre dichos índices y las variables socioeconómicas, tanto a nivel nacional como entre países.Se analizaron los datos de 105 162 hogares en el año 2000 y 144 018 en el año 2010. Entre el 2000 y 2010, la cobertura doméstica de sal suficientemente yodada aumentó un 6,1% (de un 46,3% a un 52,4%) de media, pero con diferencias regionales: la cobertura cayó un 13,0% (de un 77,5% a un 64,5%) en la República Centroafricana, pero mejoró un 40,4% (de un 22,2% a un 62,6%) en Sierra Leona. Las mejoras de la cobertura fueron mayores en zonas rurales y entre los hogares más pobres, pero las disparidades socioeconómicas nacionales se mantuvieron. Había una pequeña relación entre los cambios de la yodación de la sal y los indicadores socioeconómicos nacionales.En general, la cobertura de sal doméstica suficientemente yodada ha aumentado durante la última década. No obstante, los cambios son muy diferentes entre países. El objetivo de la yodación universal de la sal sigue siendo lejano en muchos países y requiere de nuevos esfuerzos por parte de los gobiernos, los organismos bilaterales y multilaterales y la sociedad civil.وصف التغييرات في مدى تيسر سبل حصول الأُسر على الملح المعزز باليود فيما يتعلق بالعوامل الاجتماعية والاقتصادية.قمنا باستخلاص البيانات الخاصة بالملح المعزز باليود المتداول في المنازل من واقع المسوحات العنقودية متعددة المؤشرات التي أُجريت بين عاميّ 2000 و2010. وفي إطار هذه المسوحات، فقد تم اختبار عينات الملح المتداول في المنازل للكشف عن درجة المعالجة باليود باستخدام أدوات موحدة لإجراء الاختبارات السريعة، التي تعطي نتائج لبيان ما إذا كان الملح لم يخضع للمعالجة باليود، أو تمت معالجته على نحو غير كافٍ (أي يحتوي على أقل من 15قمنا بتحليل البيانات الصادرة عن 105 162بشكل إجمالي، زادت نسبة الحصول على الملح المعزز باليود المتداول في المنازل بشكل كافٍ على مدار العقد الماضي. ومع ذلك، فقد تباينت التغييرات بشكل كبير بين الدول. ولا يزال الهدف من معالجة الملح باليود بعيد المنال بالنسبة للعديد من البلدان ويتطلب بذل جهود جديدة من جانب الحكومات، والوكالات الثنائية ومتعددة الأطراف، والمجتمع المدني.旨在说明家用碘盐普及情况的变化与社会经济因素的相关性。.我们从 2000 年至 2010 年进行的多指标类集调查中提取了家庭摄取碘盐的数据。作为调查的一部分，通过标准化的快速检测试剂盒检测家用盐，验证是否为碘盐、碘含量不足，少于 15 ppm 或充分加碘（超过 15 ppm）。 考虑到调查抽样权重，我们计算了 2000 年至 2010 年家庭食盐加碘指数。 我们研究了在国家内部和国家之间这些指标与社会经济变量的相关性。.我们分析了从 2000 年的 105 162 户家庭到 2010 年的 144 018 户家庭的调查数据。在 2000 年至 2010 之间，充分加碘盐的覆盖率上升了 6.1%（从 46.3% 到 52.4%），但是仍有地区差异：中非共和国充分含碘盐的覆盖率下降了 13.0％（从 77.5％ 到 64.5％），塞拉利昂的覆盖率却上升了 40.4％（从 22.2％ 上升到 62.6％）。农村地区和最贫困家庭充分含碘盐覆盖率提高了，但是国家内部的社会经济差距依然存在。 加碘盐的变化与国家社会经济指标之间的关联性不强。.总而言之，过去十年充分含碘的家用盐覆盖率上升了。 然而，不同国家之间变化的差异很大。 对于许多国家而言，全民食盐加碘的目标仍然遥不可及，需要政府、双边和多边机构以及民间社团作出新的努力。.Описать изменения, произошедшие в семьях в отношении доступа к иодированной соли в связи с социально-экономическими факторами.Данные по потреблению иодированной соли семействами были взяты из многоиндикаторных кластерных обследований, проведенных в 2000 и 2010 годах. В рамках этих обследований образцы соли, употребляемой в домашнем хозяйстве, проверялись на содержание иода с помощью стандартных наборов для экспресс-тестирования, которые показывают, является ли соль неиодированной, недостаточно иодированной (менее 15 частей на миллион) или достаточно иодированной (более 15 частей на миллион). С учетом весовых коэффициентов пробы были рассчитаны показатели йодирования домашней соли в 2000 и 2010 годах. Были изучены связи между этими показателями и социально-экономическими переменными как внутри стран, так и между странами.Нами были проанализированы данные для 105 162 семейств в 2000 году и для 144 018 семейств в 2010 году. В период между 2000 и 2010 годами доля семейств, пользовавшихся достаточно иодированной солью, выросла в среднем на 6,1% (с 46,3 до 52,4%), но при этом были выявлены региональные отличия: доля таких семейств упала на 13% в Центральноафриканской Республике (с 77,5 до 64,5%), но выросла на 40,4% (с 22,2 до 62,6%) в Сьерра-Леоне. Улучшение было заметнее в сельской местности и среди самых бедных семейств, но при этом сохранялось неравенство социально-экономических показателей внутри страны. Между социально-экономическими показателями на национальном уровне и изменениями в потреблении йодированной соли была выявлена слабая взаимосвязь.В целом доля семейств, использующих достаточно иодированную соль, за последнее десятилетие выросла. Однако от страны к стране изменения значительно варьировались. Многие страны все еще далеки от достижения цели всеобщего обеспечения иодированной солью, и для этого требуется возобновление работы со стороны правительств, двусторонних и многосторонних учреждений и гражданского общества.

phylaxis of endemic goiter in Switzerland. Transactions of the Third International Goiter Conference 1983;64. 6 Costa A, Cottino F, Mortara M, Vogliazzo G. Endemic cretinism in Piedmont. Panminerva Med 1964;6:250. 7 Connolly KJ, Pharoah POD, Hetzel BS. Fetal iodine deficiency and motor performance during childhood. Lancet 1979;314:1149–51. 8 Pharoah POD, Connolly KJ. A controlled trial of iodinated oil for the prevention of endemic cretinism: a long-term follow-up. Int J Epidemiol 1987;16:68–73. 9 Pharoah POD, Connolly KJ, Ekins RP, Harding AG. Maternal thyroid hormone levels in pregnancy and the subsequent cognitive and motor performance of the children. Clin Endocrinol 1984;21:265–70. 10 Pharoah P, Connolly K, Hetzel B, Ekins R. Maternal thyroid function and motor competence in the child. Dev Med Child Neurol 1981;23:76–82. 11 Pharoah POD, Hornabrook RW. Endemic cretinism of recent onset in New Guinea. Lancet 1974;304:1038–41. 12 Nelson KB, Ellenbergh JH. Antecedents of cerebral palsy. Multivariate analysis of risk. N Engl J Med 1986; 315:81–86. 13 Nelson KB. What proportion of cerebral palsy is related to birth asphyxia. J Pediatr 1988;12:572–74. 14 Pharoah POD, Adi Y. Consequences of in-utero death in a twin pregnancy. Lancet 2000;355:1597–602. 15 Pharoah POD, Cooke RWI. A hypothesis for the aetiology of spastic cerebral palsy—the vanishing twin. Dev Med Child Neurol 1997;39:292–96. 16 Pharoah POD. Fetal death registration in multiple births: anomalies and clinical significance. Twin Res Hum Genet 2006;9:587–90. 17 Croen LA, Grether JK, Curry CJ et al. Congenital abnormalities among children with cerebral palsy. More evidence for prenatal antecedents. J Pediatr 2001;138: 804–12. 18 Pharoah POD. Prevalence and pathogenesis of congenital anomalies in cerebral palsy. Arch Dis Child Fetal Neonatal Ed 2007;92:F489–93. 19 Pharoah POD, Dundar Y. Monozygotic twinning, cerebral palsy and congenital anomalies. Hum Reprod Update 2009; 15:639–48.

Endemic cretinism includes two syndromes: a more common neurological disorder with brain damage, deaf mutism, squint and spastic paresis of the legs and a less common syndrome of severe hypothyroidism, growth retardation and less severe mental defect. Both conditions are due to dietary iodine deficiency and can be prevented by correction of iodine deficiency before pregnancy. Endemic cretinism is now included in the spectrum of the effects of iodine deficiency in a population termed the 'iodine deficiency disorders (IDDs)', which also includes a wide range of lesser degrees of cognitive defect that can be prevented by the correction of iodine deficiency. Iodine deficiency is now recognised by the World Health Organization (WHO) as the most common preventable cause of brain damage with in excess of 2 billion at risk from 130 countries. A global United Nations (UN) programme of prevention has achieved 68% household usage of iodised salt by the year 2000 compared with less than 20% prior to 1990.

The Medical Journal of Australia ISSN: 0025729X 4/18 December 2006 185 11/12 646-650 ©The Medical Journal of Australia 2006 www.mja.com.au Power of One the University of Adelaide (1953–1959). A grea clinical teacher with a passionate interest in medica was an inspiration to me. I graduated fr the University of Adelaide at the Early in my course, I had enlisted in the Royal A Force, but after being diagnosed with pulmonary tu 1945, I was unable to undertake military service.

This is an edited version of the 2002 Garran Oration presented to the National Conference held in Adelaide on 13 November 2002. Dr Hetzel indicated in his address that he was pleased to respond to the challenge of the conference title ‘Powerful Connections’ but added ‘and the Challenge of Change’. Dr Hetzel was joined in the Garran Oration by Mr James Fitzpatrick who delivered an address in verse (see Conference Papers ‘Powerful Connections’, 13–16 November 2002, IPAA).

In spite of much effort over the past 25 years, the life expectancy of the indigenous people remains nearly 20 years behind the non-Aboriginal white population of Australia. These figures compare unfavourably with the improved life expectancy over the past 25 years of other indigenous peoples, such as the New Zealand Maori and the American Indian populations. By 1990-94, the average Australian indigenous all-cause mortality rate was 1.9 times the Maori rate, 2.4 times the US indigenous rate and 3.15 times the all-Australian rate. The persistence of this discrepancy in Australia is obviously a matter of great concern. There is clearly a gap between available knowledge and its application. Some indication of the possibility of reversal of the current situation is given by a recent report of the beneficial impact of the Homelands Movement on Health Outcomes in Central Australian Aborigines. The study compared the prevalence of obesity, hypertension and diabetes in two groups of Aboriginal adults: those living in homelands versus those living in centralized communities in Central Australia. Baseline studies revealed a lower prevalence of diabetes, hypertension and obesity in the homelands group, compared with those living in centralized communities. They were also less likely to die and less likely to be hospitalized for any cause, particularly infections, injury involving alcohol and other injury. Mean age at death was 58 and 48 years for the residents of homelands and centralized communities, respectively. The benefits were most marked in young adults. It is suggested that the homelands communities have a greater degree of control of their own lives than those living in the centralized communities and this may be an important factor in their improved health status. Improvement in indigenous health should be one of the key issues of reconciliation. Priorities include community control of Aboriginal Health Services under the National Aboriginal Community Controlled Health Organisation (NACCHO), throughout Australia, a greater priority for prevention and public health services (housing, water supply and environmental services) education and economic issues, improved training of indigenous health professionals and increased funding. A national professional organization including NACCHO needs to be established to bridge the big gap between available knowledge and its application for the benefit of the indigenous people of Australia.

One hundred years of European nationhood is no more than a blink in the long life of Indigenous Australia. Yet, even within half that short interval, there is plenty for reflection, pleasure and regret.

The effects of iodine deficiency on growth and development are known as the iodine deficiency disorders (IDDs). Most common is goitre at all ages, but most significant are the effects on brain development during pregnancy. The major effect of iodine deficiency is the clinical syndrome of endemic cretinism characterised in its fully developed form by mental defect, deaf mutism and spastic diplegia. This condition can be totally prevented by correction of the iodine deficiency before pregnancy. There is considerable variation in the degree of brain damage that occurs due to iodine deficiency in a given population. A meta-analysis of studies comparing iodine deficient populations with appropriate control groups reveals a mean loss of 13.5 IQ points. Experimental studies in the sheep, rat and marmoset confirm the effect of iodine deficiency on foetal brain development. They show that the effect is due to a slowing of neuroblast multiplication and differentiation and a consequent effect on neuroglial development. Iodine deficiency is now recognised as the most common cause of preventable brain damage in the world today. In 1990, the elimination of iodine deficiency as a cause of brain damage by the year 2000 was accepted by the UN system and substantial progress has been made since 1990 with the mass correction of iodine deficiency through Universal Salt Iodisation (USI).

762 International Council for Control of Iodine Deficiency Disorders, C/Centre for Health Promotion, Women’s and Children’s Hospital, 72 King William Road, North Adelaide, SA 5006, Australia. E-mail: iccidd@a011.aone.net.au made up of scientists and public health professionals from a range of disciplines available to assist national programmes; (iii) The development of effective national programmes through the UN System.

Mild iodine deficiency during pregnancy can have significant effects on fetal development and future cognitive function. The purpose of this study was to characterise the iodine status of South Australian women during pregnancy and relate it to the use of iodine-containing multivitamins. The impact of fortification of bread with iodized salt was also assessed. Women (n = 196) were recruited prospectively at the beginning of pregnancy and urine collected at 12, 18, 30, 36 weeks gestation and 6 months postpartum. The use of a multivitamin supplement was recorded at each visit. Spot urinary iodine concentrations (UIC) were assessed. Median UICs were within the mildly deficient range in women not taking supplements (

Iodine deficiency is the most common preventable cause of brain damage with more than 2 billion people from 130 countries at risk. The global problem of iodine deficiency has been redefined by a readily transmitted population concept, with an easy acronym - the concept of the iodine deficiency disorders (IDD) - referring to all the effects of iodine deficiency in a population, that can be totally prevented by correction of iodine deficiency with special emphasis on brain damage and not just to goitre and cretinism (1983). This was followed by the creation of the International Council for Control of Iodine Deficiency Disorders (ICCIDD) supported by WHO and UNICEF with 700 multidisciplinary professionals from more than 100 countries, committed to providing technical assistance to national programs for the elimination of IDD (1986). The WHO policy of Universal Salt Iodization (USI) has been widely adopted which requires iodization of all food for human and animal consumption by the use of iodized salt (25-40 mg I/kilo). Simple practical methods for monitoring - by the measurement of salt iodine and urine iodine were developed and promoted on a large scale with the technical assistance of the ICCIDD.

The WHO estimates one billion people to be at risk of iodine deficiency disorders of which mental defect is the most significant feature. Of these, 20 million are estimated to be suffering from some degree of preventable mental defect due mainly to the effects of iodine deficiency in pregnancy. The elimination of iodine deficiency disorders as a public health problem by the year 2000 has been accepted by the UN system at the World Summit for Children (1990) and the World Health Assembly (1990). In the light of the remarkable progress of national IDD control programs since 1985 there is justifiable confidence that this objective can be realised.

The establishment of the essential link among iodine deficiency, thyroid function and brain development has emerged from a fascinating combination of clinical, epidemiologic and experimental studies. The central human phenomenon that focuses this relationship is the condition of endemic cretinism, described from the Middle Ages and characterized in its fully developed form by severe brain damage, deaf mutism and a spastic state of the hands and feet. The demonstration of the prevention of cretinism in a double-blind controlled trial with injections of iodized oil in Papua New Guinea (1966-1970) established the causal role of iodine deficiency in cretinism by an effect on the developing fetal brain. Cretinism could not be prevented unless the iodized oil was given before pregnancy. Iodine deficiency is now regarded by the WHO as the most common preventable cause of brain damage in the world today, with at least 30 million suffering from this preventable condition. Since 1986 the international NGO, the International Council for Control of Iodine Deficiency Disorders, has worked closely as an expert group with WHO and UNICEF in assisting countries with a program of universal salt iodization for the elimination of iodine deficiency as a cause of brain damage by the year 2000. In 1996, WHO reported that 56% of the population of 83 developing countries now had adequate access to iodized salt. This represents an increase of 750 million since 1990 with protection of 12 million children.

This chapter reviews the clinical aspects, epidemiology, pathogenesis and the progress made toward global elimination of brain damage caused by iodine deficiency. Iodine deficiency is recognized by WHO as the most common cause of preventable brain damage, with an at-risk population in excess of 2 billion from 130 countries. The most severe effect is endemic cretinism, which is characterized by mental defect, deaf mutism and spastic diplegia. This condition is not reversible, but can be completely prevented by correction of iodine deficiency before pregnancy. The effects of iodine deficiency on the brain have been confirmed by animal studies in sheep, rats and the marmoset monkey. There is considerable variation in the effects of iodine deficiency on brain development, with a mean loss of 13.5 IQ points in an iodine-deficient population. Since 1990, there has been a global program for the elimination of brain damage due to iodine deficiency. By 2000, 68% of the population at risk had been covered by USI, which requires all salt for human and animal consumption to be iodized with potassium iodate at a level of 20–40 mg iodine/kg of salt.

The International Council for Control of Iodine Deficiency Disorders (ICCIDD) consists of a multidisciplinary global expert network of over 700 professionals from more than 100 countries with an official relationship with the World Health Organization (WHO). This network includes scientists, public health administrators, technologists, communicators, economists, salt producers and other experts, who are committed to assisting national governments and international agencies in the development of national programs for the elimination of brain damage due to iodine deficiency. The ICCIDD has 40 members. The Board of Directors meets annually, usually in conjunction with a regional meeting or special workshop. The ICCIDD has provided scientific leadership in a series of meetings with the WHO and UNICEF concerned with different technical aspects of control programs. It has played a significant role in the global program for the elimination of brain damage due to iodine deficiency, in collaboration with the WHO and UNICEF. Political support has come through the UN System—the World Summit for Children. Funding support has been provided by the WHO, UNICEF, the World Bank, and the bilateral aid agencies (AusAID, CIDA, the Netherlands, Sweden and USAID) with the participation of the governments of IDD-affected countries.

The importance of communication in public health is described with reference to recent experiences in Australia where good progress has been made with certain major public health problems. There has been a 30% fall in road accident deaths and a 40% fall in deaths from coronary heart disease, and a smoke free environment has been established in public places and in the work place. These successes depended on effective communication based on appropriate data. Evaluation data have also been used to keep the public informed and to reinforce the message. The cooperation of the media has been most important in stimulating a new awareness of health and the opportunities for self help and community initiatives. In central Australia, new initiatives involving the Central Australian Aboriginal Congress have led to an improvement in the health of Aborigines, the training of Aborigines as health workers and the development of a Centre for Appropriate Technology at the Alice Springs College of Technical and Further Education. At the international level, Australia sponsored a World Health Assembly resolution in 1986 calling for the elimination of iodine deficiency disorders. With the support of the Australian International Development Assistance Bureau and the United Nations Children's Fund (UNICEF), an international expert group of scientists and public health professionals, the International Council for Control of Iodine Deficiency Disorders (ICCIDD), based in Adelaide, has been able to work with the World Health Organization (WHO) and UNICEF in the development of an international public health programme aimed at eliminating iodine deficiency disorders by the year 2000. The ICCIDD is a new model for communication and action in international health which is now being advocated for other areas.

This chapter on nutritional epidemiology illustrates the application of epidemiology to two conditions. One is associated with undernutrition — the relation of iodine deficiency to fetal brain damage. The other is associated with overnutrition — the fall in mortality due to coronary heart disease.

The paper of Vanderpump indicates the new frontier in the cause of the elimination of iodine deficiency. It is the challenge of children pointed out by Labouisse of UNICEF in 1978 when he stated at a goitre meeting in South America, ‘Iodine deficiency is so easy to prevent that it is a crime to let a single child be born mentally handicapped for that reason’. In children the problem is now being defined by the results of psychological assessment in conjunction with measurement of urine iodine excretion. Vanderpump refers to WHO estimates that worldwide 2 billion people including 285 million schoolage children still have iodine deficiency despite major national and international efforts to increase iodine intake primarily through the voluntary or mandatory iodization of salt. 1,2

Iodine deficiency is the most common preventable cause of brain damage. WHO estimates that some 2.2 billion people are at risk from iodine deficiency in 130 countries. A programme of universal salt iodization was established in 1994 with the aim of eliminating the problem by 2000. This paper reports progress in this field, with particular reference to the primarily scientific role of the International Council for Control of Iodine Deficiency Disorders, a nongovernmental organization founded in 1986. It is now a multidisciplinary network of 600 professionals in 100 countries.

The term “iodine deficiency disorders” (IDD) is now used to denote all the effects of iodine deficiency on growth and development, particularly brain development, that can be prevented by correction of iodine deficiency . In the past, the term “goitre” has been used for many years to describe the effects of iodine deficiency. Goitre is indeed the obvious and familiar feature but our knowledge has greatly expanded in the last 25 years so that it is not surprising that a new term is needed. The term IDD has now been generally adopted in the field of international nutrition and health. This reconceptualisation has been one factor in securing much more attention to the problem of iodine deficiency in the last 10 years.

The United Nations and other international organisations, in cooperation with national governments, aim to eliminate this major cause of fetal brain damage by the year 2000.

Iodine deficiency is by far the most common preventable cause of mental deficits in the world. The evidence for this statement has emerged from a variety of disciplines, including epidemiology, end...

SOS for a Billion - the nature and magnitude of iodine deficiency disorder Recent progress in the elimination of iodine deficiency disorders The conquest of iodine deficiency through a global partnership of people, governments, international agencies, the salt industry and Kiwanis International Measurement of iodine deficiency disorders The iodization of salt for the elimination of iodine deficiency disorders The use of iodized oil and other alternatives for the elimination of iodine deficiency disorders The economic beenefits of the elimination of IDD The process of communicating the message Planning and managing national programmes for the elimination of iodine deifiency disorders in Asia, Latin America, Africa Role of international agencies - UNICEF, WHO The role of Kiwanis International Iodine deficiency disorders in Europe, Latin Amerca, Southeast Asia IDD in Africa IDD in the Middle East IDD in China Monitoring and verification of the progress towards the elimination of IDD by the year 2000

Studies have been carried out to investigate the role of maternal and fetal thyroid function in the effects of iodine deficiency on fetal brain development in sheep. Iodine deficiency was established with an especially prepared low-iodine diet of maize and pea pollard. The iodine-deficient sheep were mated and at the end of the second trimester of pregnancy (100 days gestation) were divided into groups which received either a sc injection of T4 or 3,5-dimethyl-3'-isopropyl-L-thyronine or an im injection of iodized oil. At 140 days gestation (10 days prior to parturition) comparison of the fetuses delivered by hysterotomy revealed that the retarded fetal brain development observed in iodine deficiency was greatly improved by T4 and by iodized oil. However, T4 and iodized oil failed to correct the reduction in the number and the increase in the length of synaptic appositions which were observed in the fetal cerebral cortex after iodine deficiency. In addition, the histological appearance of the fetal thyroid gland and the levels of plasma thyroid hormones were restored to normal. The administration of 3,5-dimethyl-3'-isopropyl-L-thyronine had no effect on the retarded fetal brain and body development of the iodine-deficient fetuses. The lack of response may be due to the inability of 3,5-dimethyl-3'-isopropyl-L-thyronine to cross the ovine placenta as no reduction in the abnormally elevated fetal plasma TSH was observed in spite of a fall in maternal plasma TSH and apparent restoration of maternal thyroid function. It is concluded that the retarded fetal brain development observed during iodine deficiency in sheep can be substantially improved by iodized oil or to a lesser extent by T4 administration at 100 days gestation and that this is dependent on the restoration of both maternal and fetal thyroid function which supports previous observations from this laboratory following fetal and maternal thyroidectomy. The persistence of some effects of iodine deficiency on the fetal brain suggests that irreversible damage may have occurred.

Foetal thyroidectomy and brain development in the sheep Sheep foetuses were surgically thyroidectomized at 50–60 days gestation, when thyroid function begins, and the pregnancy was then allowed to continue until 90, 120 or 150 days (term). At these times the foetuses were removed by caesarean delivery, exsanguinated, weighed and dissected. The central nervous system was divided—cerebral hemispheres, brain stem, cerebellum and spinal cord for subsequent analysis. Comparison was made with sham operations on seven foetuses. Thyroidectomy led to a fall in body weight (24.77;) and brain weight (11.7%) at 120 days and 150 days, 31.1% and 24.5% respectively. The hemispheres showed the greatest change and the cerebellum the least. DNA and protein contents were reduced in the hemispheres and cerebellum at 150 days, while in the brain stem and spinal cord the DNA content was not significantly affected. Protein content was, however, reduced indicating a reduced cell size, but not a reduced cell number as in the other two regions. Somatic changes included reduced wool growth, delayed osseous development in the limbs (X-ray assessment) a reduced heart weight (39.1%) and an increased pituitary weight (48.1%). The thyroidectomized lambs failed to survive for more than a few hours after birth or caesarean delivery at 150 days. The findings indicate significant effects of foetal thyroidectomy on brain development in the sheep late in pregnancy along with other evidence of foetal hypothyroidism.

The pattern of normal foetal brain development has been described for the Merino sheep. Controlled flock matings were used and foetuses removed by hysterotomy at 40, 54, 67, 81, 90, 95, 109, 121 and 150 days of gestation. Lambs at 7 days after birth and adults were also studied. The CNS was dissected, separated and weighed as four segments--cerebral hemispheres, brain stem, cerebellum and spinal cord. Determinations of DNA, RNA, protein, cholesterol and water content were subsequently carried out on each segment. Brain weight increased from 0.264 g (40 days) to 52.74 g at 150 days. The ratio to body weight decreased from 6.7% (40 days) to 1.5% (150 days). DNA increased more rapidly from 40 to 90 days in the cerebral hemispheres and brain stem than in the cerebellum and spinal cord and this increase preceded the main increase in weight. Increases in cholesterol and decreases in water content were also more marked in the cerebral hemispheres and brain stem. Increase in brain weight occurred in two phases, one up to 90 days followed by a more rapid and larger increase after 90 days which continued to birth. These two phases appear to reflect an increase in neuroblast multiplication followed by neuroglial multiplication and myelination respectively. At birth, brain weight had reached 50% of adult size, the cerebral hemispheres 52% of adult size, the cerebellum 40% and spinal cord 40%. The relative maturity of the brain at birth justifies the classification of the sheep as a prenatal brain developer.

Epidemiological studies have been reviewed which provide suggestive evidence of an association between the fall in coronary heart disease mortality in the U.S.A. and Australia since 1967, characterized by a fall in sudden deaths, to the increase in polyunsaturate fat consumption that has occurred in both countries since 1960. This association led directly in the same institution to carefully designed experimental studies undertaken in the rat, and a non-human primate, the marmoset ( Callithrix jacchus jacchus ) with a heart and lipid metabolism more closely resembling that of man. In both animal species, a vegetable fat diet had a protective effect against the increase in contractility of isolated papillary muscles induced by age, the addition of animal fat, or by isoprenaline in vitro . Similar effects were observed following coronary artery ligation, where the extent of dysrhythmia was greatly reduced by supplementing the diet with a linoleic acid rich vegetable oil. It is concluded that the combination of epidemiological and experimental evidence indicates a protective effect of dietary polyunsaturates against sudden cardiac death. This work illustrates the value of the integration of epidemiological and experimental approaches to the aetiology of disease.

A comparison has been made of the recent changes in coronary heart disease mortality in Australia, the USA, and in the United Kingdom (England and Wales). Sharp declines in mortality dating from 1966 in Australia and from 1968 in the USA in both sexes contrast with a persistent increase in men in England and Wales until 1972 (after which a sight fall occurred) and a consistent slight fall in women since 1950. An investigation has been made of changes in 3 major risk factors-hypertension, cigarette smoking and diet in the 3 countries in an attempt to determine to what extent such changes might correlate with the different patterns of mortality. There has been a progressive and similar fall in mortality due to hypertension in both sexes in all 3 countries since 1950. There was a rise in cigarette smoking in all 3 countries from 1947 followed by a fall in the USA from 1963 and a more recent fall in men in Australia. There has been a levelling off of smoking in the United Kingdom in middle-aged and older men but not in women where smoking rates have increased from 1950 since when there has been a progressive slight fall in overall coronary heart disease mortality (although there is evidence of a recent rise in younger women.) Changes in dietary constituents (meat, eggs, milk and cheese, butter or margarine) have been examined by reference to aggregate consumption data. In Australia and the USA increases in vegetable fat consumption have occurred since 1950 with a reduction in animal fat in Australia but not in the USA. In the United Kingdom increases in vegetable fat have not been observed while there has been some increase in animal fat. It is concluded that the different patterns of coronary heart disease mortality in the 3 countries do correlate to some extent with changes in diet and cigarette smoking.The authors compare recent trends in coronary heart disease mortality in Australia, the United States, and England and Wales. Changes in hypertension, cigarette smoking, and dietary constituents are analyzed by age and sex to determine the extent of correlation with differences in mortality patterns

Global descriptive, epidemiological studies have established the relation of iodine deficiency to endemic cretinism which, in its fully developed form, is characterized by mental deficiency, deaf mutism and spastic diplegia. However, a second less common variant--myxedematous or hypothyroid cretinism--is characterized by severe hypothyroidism with dwarfism. Mixed forms occur. It has been shown that both conditions can be prevented by correction of the iodine deficiency before pregnancy. Cretinism and development--now termed iodine deficiency disorders (IDD). A number of recently developed animal models establish the effect of severe iodine deficiency on brain development. These include the rat, the marmoset monkey and the sheep. These models are all characterized by the production of severe maternal and fetal hypothyroidism which is associated with effects on the maturation of the cerebral cortex and cerebellum. There was a reduced brain weight with a reduced number of cells as indicated by reduced DNA, a greater density of cells in the cerebral cortex and reduced cell acquisition in the cerebellum. Studies of the mechanisms involved have been carried out in the sheep. The findings reveal significant, though less severe, effects of fetal thyroidectomy (late gestation) and a significant effect of maternal thyroidectomy on brain development in mid-gestation. A combination of maternal and fetal thyroidectomy has similar but more severe effects than iodine deficiency. In the light of current knowledge of the embryology of the brain it is suggested that the critical time for the effect of iodine deficiency is the mid-trimester (14-18 weeks) when the neurons of the cerebral cortex and basal ganglia are formed and could be damaged by the effect of iodine deficiency on maternal thyroid function. There is now recent evidence indicating transfer of maternal thyroxine across the placental barrier early in pregnancy. In this way, neurological cretinism might be produced. Impaired fetal thyroid function would follow in the third trimester and augment the effect of reduced maternal thyroid function. Impaired fetal thyroid function alone could produce the hypothyroid form of cretinism. Further experimental studies, particularly into the postnatal period, are required to substantiate these suggestions. Apart from this, further study of the effects of iodine deficiency on brain development at the subcellular and cellular levels are likely to be most productive.

Iodine deficiency is now recognized as a major international public health problem. It is estimated that 800 million people may be at risk of the effects of iodine deficiency. In humans, the effects occur at all stages of development: the fetus, the neonate, the child and adult. The effects are now denoted by the term iodine deficiency disorders (IDD). They include miscarriages, stillbirths, congenital anomalies, as well as the more familiar goiter, cretinism, impaired brain function, and hypothyroidism in children and adults. In domestic animals, reproductive failure has been reported with the production of aborted, stillborn and weak calves. Experimental studies in animal models have been reviewed to provide evidence of the mechanisms involved, particularly in relation to brain development. The findings in three different species (rat, sheep, monkey) indicate that the effects are mediated by a combination of maternal and fetal hypothyroidism, the effect of maternal hypothyroidism being earlier than the onset of fetal thyroid secretion. The findings suggest that iodine deficiency has an early effect on neuroblast multiplication and, if so, this could be important in the pathogenesis of the neurological form of endemic cretinism. The assessment of the full effects of iodine deficiency on the brain requires further studies in the postnatal period to determine the duration of these effects.

SUMMARY Patients with endemic goitre in an iodine deficient area in the Territory of Papua and New Guinea (TPNG) have very little clinical evidence of hypothyroidism although serum thyroxine (T4) levels are usually very subnormal. The activities of T4-binding proteins in both goitrous and non-goitrous iodine deficient TPNG subjects were therefore investigated but no overall deficiencies were found to account for the low T4 levels. The mean serum T4-binding pre-albumin (TBPA) level (169 μg/100 ml as T4-binding capacity) was less than the level seen in Australian subjects (187 μg/100 ml); however, this decrease was counteracted by the increase in T4-binding globulin (TBG) level (27±3 μg) in iodine-deficient TPNG compared with 19±9 μg in Australia. Measurements of TBG and TBPA levels were also made during pregnancy in TPNG subjects, and found to increase to the same extent as in pregnancy in Australian subjects. This suggests that the pathogenesis of endemic cretinism (in TPNG) is dependent on some factor other than TBG deficiency during pregnancy.

Thyroid status is known to have an important bearing on the ability of a woman to conceive, and to bring a normal infant to term. Thyroid status has changed in a number of previously iodine deficient countries as a result of recent iodization programmes. In this study, examination has been made of changes in the rates of two pregnancy outcomes in Tasmania, a State of Australia, namely, stillbirth and infant death due to congenital anomalies. Tasmania began iodine supplementation in 1950. Stillbirth rates declined more rapidly than in Australia as a whole, but show a peak associated with the peak of iodine-induced thyrotoxicosis in 1966. Congenital anomalies causing death show an initial rise in the early 1950s. It is suggested that this is due to persistence of iodine deficiency in the foetus after maternal iodine status improved sufficiently to allow term delivery of a live infant. The later fall coincides with the reaching of reproductive age by the first cohort of Tasmanian women who had been iodine sufficient since childhood, who would therefore not deprive their own foetus of iodine. Examination of trends in New Zealand, Switzerland and Finland, which have each introduced iodization programmes, confirms the largely beneficial effect of iodine supplementation on the rate of infant death due to congenital anomalies.

Two obvious forms of student "wastage" are academic failure and withdrawal from university. In this prospective cohort study of 2,041 first-year students at Monash University, the relationship of these two events to mental health, university life-stress and other variables is examined. Four factors found to be strongly related to first-year academic failure are mental illness at university a high level of life-stress, poor secondary school academic record, and an extroverted personality. Withdrawal from university during first year is frequently preceded by poor mental health, high life-stress and loneliness. Withdrawal during second year is strongly associated with first-year academic failure and mental illness. The significance of these findings is discussed, and comparisons are made with overseas studies.

Studies of the health effects of a daily physical activity programme have been carried out in 10-year-old school children in Adelaide, South Australia. In the first phase (1978) observations on endurance fitness, four skin folds, blood pressure and blood lipids were made before and after a randomized trial over a period of 14 weeks. Comparisons were made on over 500 children drawn from classes in seven Primary schools involved in an endurance fitness programme (1 1/4 hours per day), a skill programme and the previous physical education programme (controls). The fitness group experienced significant gains in physical work capacity (PWC) and showed significant decreases in body fat compared to the other two groups. No significant differences were observed in plasma cholesterol, triglycerides and HDL cholesterol. Subsequently in the second phase (1980) observations were made on a group of 216 10-year-old children who had already experienced two years of the physical activity programme adopted after phase one. Comparison with the observations in the 10-year-old children in 1978 made prior to the intervention revealed significantly smaller skin folds and greater PWC, with lower blood pressure reaching statistical significance for diastolic pressure in boys. The findings suggest beneficial effects on health of daily physical activity programmes within existing primary school curricula. There was no evidence of any loss of academic performance as measured by arithmetic and reading tests in spite of 45-60 minutes' loss of formal teaching time each day.

Iodized oil was administered as a single intramuscular injection to pregnant iodine-deficient ewes at 100 days gestation and the subsequent growth of their fetuses compared with that of fetuses of severely iodine-deficient ewes and of iodine-replete ewes, all of which were fed the same low-iodine diet. The administered iodine produced a remarkable improvement in thyroid function and physical appearance of the fetuses, accompanied by an increase in brain growth and to a lesser extent in body growth, which at 140 days was only slightly (but significantly) less than that of the controls. There was restoration of the number of cells (DNA) and myelination (cholesterol/DNA) in the cerebellum and cerebral hemispheres which suggests a catch-up of neuroblast development during pregnancy. Histological examination, however, revealed that counts of synapses (density) in the cerebral cortex after iodized oil were still less than those of the control fetal brains. The relevance of these findings to the effects of iodine deficiency on human brain development is discussed.

Disorders resulting from severe iodine deficiency affect more than 400 million people in Asia alone. These disorders include stillbirths, abortions, and congenital anomalies; endemic cretinism, characterised most commonly by mental deficiency, deaf mutism, and spastic diplegia and lesser degrees of neurological defect related to fetal iodine deficiency; and impaired mental function in children and adults with goitre associated with subnormal concentrations of circulating thyroxine. Use of the term iodine deficiency disorders, instead of "goitre", would help to bridge the serious gap between knowledge and its application. Iodised salt and iodised oil (by injection or by mouth) are suitable for the correction of iodine deficiency on a mass scale. A single dose of iodised oil can correct severe iodine deficiency for 3-5 years. Iodised oil offers a satisfactory immediate measure for primary care services until an iodised salt programme can be implemented. The complete eradication of iodine deficiency is therefore feasible within 5-10 years.

The application of the technique of paper chromato graphy and the use of radioactive iodine resulted in the demonstration of thyroxine (T4) as the major iodine-containing component in the plasma (Laidlaw, 1949 ; Taurog et al., 1950). Thyroxine was also found to be the major circulating iodine compound in thyro toxicosis by Rosenberg (1951). In 1952 Gross and Pitt-Rivers demonstrated the presence of 3-5-3'-L triiodothyronine (T,) in the serum of four thyrotoxic patients and two patients with thyroid carcinoma. They suggested that there was no qualitative difference beween the iodine compounds present in the circulation of normal and thyrotoxic subjects. Subsequent studies (Benua and Dobyns, 1955 ; Dingledene et al., 1955 ; Arons and Hydovitz, 1959) have confirmed the findings of Gross and Pitt-Rivers in thyrotoxicosis. T4 was found to be the major component, while T3 was detected in a variable proportion of thyrotoxic patients after radio active iodine (i:uI) administration. The presence of triiodothyronine in the plasma of both normal and thyrotoxic subjects was confirmed by Maclagan et al. (1957) using a chemical method of detection. This method made use of the very sensitive ceric-sulphate-arsenious-acid catalytic system for detecting iodine. Their finding eliminated the possibility that the presence of triiodothyronine might have been artifactual owing to radiation damage to the thyroid gland from the radioactive iodine employed in the earlier studies. Farran et al. (1959) using "semi-tracer" doses of radioiodine, reported the presence of iodotyrosines in the plasma of approximately 50% of cases of thyrotoxicosis. The patients whose plasma contained iodinated tyro sines showed a greater mean gland weight and were more resistant to radioactive iodine therapy than those without iodinated tyrosines. The presence of iodo tyrosines was confirmed by the use of chemical methods (Bird and Farran, 1960). This finding raised the possi bility of an abnormal thyroid secretion in thyrotoxicosis. More recently still, two separate groups of investigators (Block et al., 1960 ; Beale and Whitehead, 1960) have reported the presence of iodotyrosines in the blood of normal subjects accounting for 35-50% of the total organic blood iodine. This finding has not been con firmed in normal animals (Pitt-Rivers and Rail, 1961). In view of these variable results and their importance for understanding the pathogenesis of thyrotoxicosis it was decided to reinvestigate the pattern of plasma hormones in normal and thyrotoxic patients. Chemical methods were used in studying plasma from normal subjects, but in thyrotoxic subjects both chemical and radioactive methods of detection were used whenever possible. Methods